Effect of E-cadherin on the proliferation,invasion and gene expression profile of gas-tric cancer AGS cells
Objective To investigate the effects of E-cadherin on the proliferation,invasion,migration,and cispla-tin(DDP)chemotherapy sensitivity of gastric cancer AGS cells,and to screen potential downstream genes and mechanisms of E-cadherin regulation.Methods The gastric cancer AGS cells(the control group)and E-cadherin overexpressing AGS cells(the E-cadherin overexpressing group)were cultured to logarithmic growth phase.CCK-8 method was used to detect cell viability in the two groups.The colony formation assay was used to detect cell proliferation.Transwell assay was used to analyze cell invasion and migration.Genechip was used to compare and analyze the changes of cell gene expression profiles in the two groups,and to screen differentially expressed genes.Bioinformatics methods were performed for Gene Ontology(GO)annotation and Kyoto Encyclopedia of Genes and Genomes(KEGG)signaling pathway enrichment analysis based on differentially expressed genes.Results Compared with the control group,the E-cadherin overexpression group showed a decrease in cell viability(between subjects effects:F=101.674,P＜0.001;within subjects effects:F=9.712,P=0.001;interaction effects:F=9.712,P=0.001),a decrease in the number of cell colonies(t=11.452,P＜0.001),and a decrease in the number of migratory and invasive cells(cell migration:t=3.994,P=0.016;cell invasion:t=2.971,P=0.041);under the action of DDP,compared with the control group,the E-cadherin overexpression group showed a de-crease in cell viability(between subjects effects:F=24.312,P＜0.001;within subjects effects:F=327.222,P＜0.001;interaction effects:F=14.445,P＜0.001),a decrease in the number of migratory and invasive cells(cell migration:t=4.253,P=0.013;cell invasion:t=3.944,P=0.017);there were 3 882 differentially expressed genes were screened after overexpression of E-cadherin,included 552 lncRNA,272 circRNAs and 3 058 mRNAs.The functions of differentially ex-pressed genes identified were mainly involved in positive regulation of GTPase activity,extracellular matrix generation,an-giogenesis according to GO annotation.KEGG analysis showed that differentially expressed genes were mainly enriched in extracellular matrix receptor interactions,mitogen-activated protein kinase signaling pathways,complement coagulation cas-cade pathways.Conclusion E-cadherin inhibits the proliferation,migration and invasion of gastric cancer cells by regula-ting genomic changes,providing a molecular basis for personalized treatment strategies of gastric cancer.
万方数据
维普
